Discover how groundbreaking research on mitochondrial fission inhibition offers new hope in the battle against hypertension triggered by angiotensin II, shedding light on potential therapeutic avenues.
– by James
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Mitochondrial fission inhibition protects against hypertension induced by angiotensin II.
Preston et al., Hypertens Res 2024
<!– DOI: 10.1038/s41440-024-01610-0 //–>
https://doi.org/10.1038/s41440-024-01610-0
This study explores the role of mitochondrial fission in hypertension and cardiovascular remodeling, proposing that inhibiting mitochondrial fission could mitigate these conditions. Using C57BL6 mice infused with angiotensin II to induce hypertension, the research demonstrates that co-treatment with the mitochondrial fission inhibitor, mdivi1, significantly reduces the development of hypertension and associated vascular remodeling. Key findings include:
– **Mdivi1’s inhibition** of vessel fibrosis and hypertrophy induced by angiotensin II.
– **Attenuation** of the decline in mitochondrial aspect ratio in the endothelial and medial layers of aortas by mdivi1.
– **Mitigation** of angiotensin II-induced cardiac hypertrophy, as evidenced by heart weight-to-body weight ratio and echocardiography.
– **Inhibition** of vasoconstriction and enhanced vascular reactivity by angiotensin II in ex vivo experiments.
– **Proteomic analysis** revealing mdivi1’s prevention of the endothelial cell hypersecretory phenotype and attenuation of periostin induction, a myofibroblast marker, in vascular fibroblasts.
This research underscores the potential of targeting mitochondrial fission as a therapeutic strategy for hypertension and cardiovascular remodeling, offering a novel approach to addressing these widespread health issues.